Neurology Flashcards

1
Q

Where in the CNS is CSF produced? Where is it absorbed?

A

Produced by choroid plexuses (mainly), ependymal cells of the ventricles, and arachnoidal membranes
Absorbed by arachnoidal villi

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2
Q

Which extraocular muscles are innervated by the oculomotor nerve?

A

Dorsal, ventral, and medial rectus

Also, parasympathetic nervous system to pupil (causes constriction)

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3
Q

Which peripheral nerve is involved in the perineal reflex arc?

A

Pudendal nerve

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4
Q

What is the primary neurotransmitter in skeletal muscle?

A

Acetylcholine

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5
Q

Damage to which area causes Horner’s syndrome? What are the clinical signs?

A

Cervical sympathetic trunk

Miosis, ptosis, enophthalmos, protrusion of the third eyelid

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6
Q

Summarize the innervation of the bladder.

A

Sympathetic innervation supplied by hypogastric nn (B2 receptors on detrusor mm cause relaxation/filling, a1 receptors on IUS cause contraction)

PS innervation by pelvic n, dominates during emptying phase/micturation

Somatic innervation by deep perineal nerve (branch of pudenal nerve) which allows for conscious control of EUS

Pontinue micturation center in brain is essential for complete emptying of the bladder

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7
Q

What is the main regulator of CSF pressure in a healthy individual?

A

Rate of CSF absorption by the arachnoidal villi (produced at a near constant rate)

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8
Q

A patient has the following signs: horizontal nystagmus with fast phase to the left, a right sided head tilt, and left-sided ataxia/CP deficits. What is the neuroanatomic localization?

A

Left side of the floculonodular lobe of the cerebellum (paradoxical vestibular disease)

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9
Q

What are the clinical signs of idiopathic head tremors?

A

Sudden onset of vertical and/or horizontal rhythmic head movements lasting from a few seconds to several hours, usually able to be distracted out of the episode

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10
Q

What are the clinical signs and signalment of cerebellitis (shaker syndrome)?

A

Sudden marked intention tremor of the head and limbs, which worsens with exercise, stress and excitement, but disappears during sleep; Classically seen in young, mature (<2 years), small white-breed dogs, particularly
Maltese terriers and West Highland white terriers, however, any breed can be affected

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11
Q

What is the clinical presentation for idiopathic trigeminal neuritis?

A

Dropped jaw (resulting from impaired muscles of mastification), trigeminal sensory deficits seen in 1/3 of dogs; concurrent facial nerve paralysis, Horner’s syndrome, or masticatory mm atrophy can occasionally be observed. Recover spontaneously in 2-4 weeks

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12
Q

Deficits to CN III cause what clinical signs?

A

Strabismus, mydriatic pupil (due to loss of PS innervation of eye)

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13
Q

What are the distinguishing characteristics of pre-ganglionic Horner’s syndrome from post-ganglionic Horner’s?

A

Pre-ganglionic: phenylephrine instilled in eye will have no effect on pupillary constriction (signifies injury to neck or brachial plexus)

Post-ganglionic: phenylephrine instilled in eye will cause pupillary dilation in ~20 minutes (most commonly due to otitis media/interna)

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14
Q

What are the two types of acetylcholine receptors?

A

Nicotinic and muscarinic

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15
Q

What are the clinical signs of cerebellar disease?

A

Normal behavior/alert, intention tremors, opisthotonous/extensor rigidity, exaggerated muscle tone/spinal reflexes, absent menace (ipsilateral)

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16
Q

What are the biopsy findings in cases of GME?

A

Perivascular infiltrates of mononuclear cells (lymphocytes, macrophages, plasma cells) in brain and/or spinal cord, primarily in white matter

17
Q

Which cranial nerves are parasympathetic?

A

III, VII, IX, X

18
Q

What does CN V innervate?

A

Motor to muscles of mastication, sensory to face

19
Q

What causes acquired polyneuropathies?

A

Acute: Coonhound paralysis (etiologic agent unknown, suspected to be auto-immune response, often have recent exposure to raccoon saliva or a virus)

Chronic: many causes endocrinopathies (diabetes mellitus, hypothyroidism, and hyperadrenocorticism), neoplasia (insulinoma, lymphosarcoma [adeno]carcinomas, and sarcomas), toxins and drugs (cisplatin, vincristine, and vinblastine), infection (Neospora caninum), immune-mediated disease (systemic lupus erythematosus [SLE] or primary immune disease against peripheral nerve myelin), and idiopathic causes (chronic axonal degeneration).

20
Q

Localize this lesion: decreased consciousness, left hemiparesis, dazzle present OS, absent PLR OS,
strabismus OS, normal menace OU.

A

Left mesencephalon (midbrain) at level of CN III nuclei?

21
Q

Localize this lesion: right hemiparesis, right head tilt, decreased CP right hind and right front.

A

Right-sided central vestibular disease (pons)

22
Q

What is seen with acquired myasthenia gravis?

A

Fatigue of palpebral reflex, skeletal muscle weakness exacerbated by activity, otherwise normal neuro exam

23
Q

What intracranial neoplasia arises from neuroepithelial cells?

A

Oligodendrocytoma

24
Q

What vitamin deficiency can lead to cervical ventroflexion in cats?

A

Thiamine (aka B1)

25
Q

How do you diagnose steroid responsive meningitis-arteritis (SRMA)?

A

Increased IgA in CSF & increased C-reactive protein (CRP) in serum

26
Q

What pathologic changes are caused on the CNS by systemic hypertension?

A

Cerebral edema, caudal displacement of the vermis, arteriolar hyalinosis, hyperplastic arteriosclerosis, ischemia, necrosis, cerebral hemorrhage

27
Q

What nerve provides PNS (parasympathetic) to the urethra?

A

Pelvic nerve